Technical Abstract:
Erwinia amylovora (Ea) utilizes a type three secretion system (T3SS) to deliver effector proteins into plant host cells. Several Ea effectors have been identified based on their sequence similarity to plant and animal bacterial pathogen effectors; however, the function of the majority of Ea effectors in host-pathogen interactions has not been characterized. Eop1 (Erwinia outer protein 1) has sequence similarity to the animal pathogen Yersinia pseudotuberculosis effector YopJ. YopJ is known to inhibit host immune responses by blocking multiple signaling pathways. In order to characterize the role of Eop1, Malling 26 apple rootstock was genetically engineered to express the Ea effector protein Eop1 under the control of an estradiol inducible promoter. Callose deposition, a classic cellular marker for defense responses, is triggered by pathogen associated molecular patterns (PAMPs). When apple was challenged with a T3SS deficient mutant of Ea273 (EaT3SS-), levels of callose deposition in leaves were significantly greater than that observed in apple leaves challenged with Ea273 wild-type (wt). When transgenic apple expressing Eop1 was challenged with EaT3SS-, callose deposition levels were reduced to levels similar to Ea273 wt. We used previous studies of Malus–Ea and Arabidopsis–Pseudomonas syringae pathosystems to identify a set of PAMP responsive candidate genes in Malus. Gene expression analysis of these candidate genes revealed Eop1’s ability to transcriptionally regulate Malus genes involved in PAMP triggered immunity. The results suggest that Eop1 functions to suppress PAMP-triggered immunity in Malus.